[NO HYPE]

Most of us are well aware of the beneficial mechanisms of nitric oxide however.... this thread is in response to all of the hype that accompanies these so-called.... "NO" products, and adresses the reasons why I feel that the hype is complete BS. It also nullifies the entire logic behind NO up-regulation in healthy adults.

The entire premise behind NO products, is NO up-regulation.... IF the NO products even aquired the ability to up-regulate endogenous NO production (wich they don't)....

It would be detrimental to our health!

In healthy adults (provided there is no shortage of the NO substrate), there is no need for NO up-regulation, and if there were a need.... it would not be possible to significantly up-regulate via the oral arginine-based "NO products", due to the p53-mediated, regulatory negative feedback loop.

I would not want to inhibit iNOS-derived, high-output NO (as it can be beneficial as well as detrimental).... I would just rather not have it up-regulated.

Here's why....


"Nitric oxide is toxic at high physiological concentration where it appears to function as a cellular effector molecule that mediates both cytostatic and cytotoxic effect." "NO is generated in the course of inflammatory and immune reactions, both by macro****es and by neutrophils. The role of these cells is quite extensive, and includes ****ocytic and non-****ocytic destruction of foreign or damaged cells. These processes involve the production of large quantities of NO, which is cytotoxic."

The enhancement of the hyperglycemic effect of S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine by vitamin C in an animal model | BioMed Central - Mirror @ Uni Potsdam




"Although NO can be cytotoxic to tumour cells (as it is to other cells), it can also act as a carcinogen."

[B]http://www.clinsci.org/cs/098/0507/0980507.pdf




"NO, a chemical radical, and its toxic derivatives can cause DNA damage and cell death in a variety of cell types. NO also has the ability to directly modify intracellular targets such as proteins and lipid-peroxidation products. NO produces cytotoxicity at high concentrations, whereas NO at lower concentrations may have the opposite effect and protect against apoptotic cell death from various stimuli. Therefore, regulation of NO production is vital for both cell survival and genome integrity. DNA damage triggers p53 protein accumulation, which produces either growth arrest or apoptosis. Exposure of cells to high NO concentrations causes DNA damage and apoptosis, and recent results have shown that NO stimulates p53 accumulation and p53-mediated apoptosis."

Up-regulation of inducible nitric oxide synthase expression in cancer-prone p53 knockout mice -- Ambs et al. 95 (15): 8823 -- Proceedings of the National Academy of Sciences




"High concentrations of nitric oxide (NO) cause DNA damage and apoptosis in many cell types. Thus, regulation of NO synthase (NOS) activity is essential for minimizing effects of cytotoxic and genotoxic nitrogen oxide species." "These genetic and functional data indicate that p53 is an important transrepressor of NOS2 expression in vivo and attenuates excessive NO production in a regulatory negative feedback loop".

Up-regulation of inducible nitric oxide synthase expression in cancer-prone p53 knockout mice.




"The enzyme nitric oxide synthase 2 (NOS2), often called inducible NOS, plays a central role in the inflammatory reactions that follow infection or tissue damage. NOS2 has been detected in virtually every cell type, and the NO it produces can perform both beneficial and detrimental actions. It is thus conceivable that regulatory mechanisms exist which control the timing and intensity of NO production by NOS2 in order to outweigh protective effects against detrimental ones."

Regulation of the expression of the inflammatory nitric oxide synthase (NOS2) by cyclic AMP.




"The aberrant production of nitric oxide (NO) contributes to the pathogenesis of diseases as diverse as cancer and arthritis.

Sustained nitric oxide production in macro****es requires the arginine transporter CAT2.




"Inducible nitric oxide synthase (iNOS) is induced by inflammatory cytokines in skeletal muscle and fat. It has been proposed that chronic iNOS induction may cause muscle insulin resistance." "These findings provide genetic evidence that iNOS is involved in the development of muscle insulin resistance in diet-induced obesity."

Targeted disruption of inducible nitric oxide synthase protects against obesity-linked insulin resistance in muscle.




"Our results show that short-term NOS2 expression enhances CD95-mediated apoptosis and T cell cytotoxicity dose dependently. Furthermore, we could show that during chronic exposure to NO, besides the primary cytotoxic NO effect, there is selection of cell clones resistant to NO that show cross-resistance to CD95-induced apoptosis and the killing by CTLs. We propose that NO production could initially act as an autocrine suicide or paracrine killing mechanism in cells undergoing malignant transformation. However, once failed, the outcome is fatal. NO promotes tumor formation by enhancing the selection of cells that can evade immune attack by acquiring apoptosis resistance."

Nitric Oxide Promotes Resistance to Tumor Suppression by CTLs.




"Nitric oxide (NO.), an important mediator of inflammation, and beta-catenin, a component of the Wnt-adenomatous polyposis coli signaling pathway, contribute to the development of cancer." "These data are consistent with the hypothesis that beta-catenin up-regulates NOS2 and suggest a novel mechanism by which the Wnt/beta-catenin signaling pathway may contribute to cancer by increasing NO. production."

Regulation of Human Nitric Oxide Synthase 2 Expression by Wnt {beta}-Catenin Signaling.




"NO synthase 2 (NOS2) plays an important role in endotoxemia through overproduction of NO".

Reduction of nitric oxide synthase 2 expression by distamycin A improves survival from endotoxemia.




"Nitric oxide (NO) production in macro****es by inducible nitric oxide synthase (NOS2) has multiple tissue damaging effects and is involved in the pathogenesis of inflammation and graft rejection." "NOS2 inhibition may explain the antinflammatory effects of HmOx induction which could also be used therapeutically in situations when NO hyperproduction leads to cytotoxic effects such as inflammation or transplant rejection."

Nitric oxide synthase inhibition by haem oxygenase decreases macro****e nitric-oxide-dependent cytotoxicity: a negative feedback mechanism for the regulation of nitric oxide production.




"Recent evidence suggests that expression of inducible nitric oxide synthase (iNOS), or Nos2 gene product, in vascular smooth-muscle cells may, in part, promote atherosclerosis by increasing local oxidative stress. We therefore hypothesized that homocysteine contributes to atherosclerosis by affecting cytokine-induced production of nitric oxide (NO) by vascular smooth-muscle cells." "These data demonstrate that exposure of vascular smooth-muscle cells to pathophysiologically relevant concentrations of homocysteine prior to cytokine stimulation leads both to an increase in NO production and to an NF-kappa B-mediated increase in Nos2 transcription. Upregulation of Nos2 may contribute to the inflammatory response that characterizes early atherogenesis and may, in part, account for the adverse vascular effects of hyperhomocysteinemia."

Homocysteine-induced nitric oxide production in vascular smooth-muscle cells by NF-kappa B-dependent transcriptional activation of Nos2.




"Increased production of nitric oxide (NO) after induction of the cytokine-inducible isoform of nitric oxide synthase (iNOS or NOS2) in cardiac myocytes and other parenchymal cells within the heart may in addition to contributing to myocyte contractile dysfunction also contribute to the induction of programmed cell death (apoptosis). To investigate the mechanism(s) by which increased NO production leads to apoptosis, we examined the role of NO in primary cultures of neonatal rat ventricular myocytes"

Cytokine-mediated apoptosis in cardiac myocytes: the role of inducible nitric oxide synthase induction and peroxynitrite generation.




"Increased NOS2 expression and NO generation may be important in the pathogenesis of RA".

Increased expression of blood mononuclear cell nitric oxide synthase type 2 in rheumatoid arthritis patients.




Elevated polyamine and nitric oxide levels (both derived from arginine) promote tumorigenesis, whereas non-steroidal anti-inflammatory drugs (NSAIDs) inhibit colorectal cancer (CRC) incidence in experimental and epidemiologic studies."

Risk and risk reduction involving arginine intake and meat consumption in colorectal tumorigenesis and survival.




"The inducible nitric oxide (NO) synthase (iNOS or NOS2) generates a prolonged release of large amounts of NO which may be cytotoxic and/or inhibit myocyte contractility. It has been suggested that this mechanism specifically contributes to heart failure caused by dilated cardiomyopathy (DCM)."

Inducible nitric oxide synthase (iNOS) in the human heart: expression and localization in congestive heart failure.

[poison]

OK, nice post. Now post the other side of the argument, someone.

NO has anti-oxidant properties, lowers blood pressure, etc.

[MaDmaN]

Originally Posted by poison

OK, nice post. Now post the other side of the argument, someone.

NO has anti-oxidant properties, lowers blood pressure, etc.

Im sure there would be some small benefit,but at what cost ?

The claims are insane and at $50-$60 at what green tea would do is crazy..I never felt a thing using any NO product other than the NO Explodes and turbo V-12 which has alot more than just 3 grams Arginine Ketogluterate..JMO

[NO HYPE]

Originally Posted by poison

OK, nice post. Now post the other side of the argument, someone.

Do you mean the other side of the argument that every company uses to promote NO products?

[V00D00]

Originally Posted by NO HYPE

Do you mean the other side of the argument that every company uses to promote NO products?

i want to see what Dr. D and Dinoiii have to say on this issue. While I tend to agree somewhat (I'm pretty much a believer in phs and phs only as a muscle building supplement) i would like to see how they break it down.
Of course nitrogen levels are important though, and I could imagine a person blowing them self away at the gym might run a negative balance.

[NO HYPE]

Originally Posted by V00D00

i want to see what Dr. D and Dinoiii have to say on this issue. While I tend to agree somewhat (I'm pretty much a believer in phs and phs only as a muscle building supplement) i would like to see how they break it down.
Of course nitrogen levels are important though, and I could imagine a person blowing them self away at the gym might run a negative balance.

I too, would like their opinion on the matter.

[Sir Savage]

I'm preparing a response right now.

[Sir Savage]

Originally Posted by NO HYPE

[B][size=+1]


"Nitric oxide is toxic at high physiological concentration where it appears to function as a cellular effector molecule that mediates both cytostatic and cytotoxic effect." "NO is generated in the course of inflammatory and immune reactions, both by macro****es and by neutrophils. The role of these cells is quite extensive, and includes ****ocytic and non-****ocytic destruction of foreign or damaged cells. These processes involve the production of large quantities of NO, which is cytotoxic."

The enhancement of the hyperglycemic effect of S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine by vitamin C in an animal model | BioMed Central - Mirror @ Uni Potsdam

This is taken from research where streptozotocin, an NO donor, was used to cause damage to beta cells!! Streptozotocin is extremely toxic and is in no way relevant to taking arginine supplements.

From the same piece of research-

"Vitamin C has been known to accelerate the decomposition of GSNO and SNAP increasing the release and availability of NO which is cytotoxic at non-physiological concentrations."

NON-physiological concentrations.

"Although NO can be cytotoxic to tumour cells (as it is to other cells), it can also act as a carcinogen."

[B]http://www.clinsci.org/cs/098/0507/0980507.pdf

Once again, this has little to do with arginine supplementation. It mainly discusses NO-donating DRUGS, production of NO, and production of NO under various disease states. Not terribly relevant to the typical supplement user.

"NO, a chemical radical, and its toxic derivatives can cause DNA damage and cell death in a variety of cell types. NO also has the ability to directly modify intracellular targets such as proteins and lipid-peroxidation products. NO produces cytotoxicity at high concentrations, whereas NO at lower concentrations may have the opposite effect and protect against apoptotic cell death from various stimuli. Therefore, regulation of NO production is vital for both cell survival and genome integrity. DNA damage triggers p53 protein accumulation, which produces either growth arrest or apoptosis. Exposure of cells to high NO concentrations causes DNA damage and apoptosis, and recent results have shown that NO stimulates p53 accumulation and p53-mediated apoptosis."

Up-regulation of inducible nitric oxide synthase expression in cancer-prone p53 knockout mice -- Ambs et al. 95 (15): 8823 -- Proceedings of the National Academy of Sciences

This is about p53 protein knockout mice!! What possible relevance does this have to healthy human subjects who take l-arginine supplements??

Elevated polyamine and nitric oxide levels (both derived from arginine) promote tumorigenesis, whereas non-steroidal anti-inflammatory drugs (NSAIDs) inhibit colorectal cancer (CRC) incidence in experimental and epidemiologic studies."

Risk and risk reduction involving arginine intake and meat consumption in colorectal tumorigenesis and survival.

I thought this would be the most relevant, but it turned out to be more irrelevancy. They used MEAT as a proxy for L-arginine consumption, and then tried to tie it to colorectal tumorigenesis, which is horrible science, IMO.

First aff, the arginine in meat is peptide bonded with other mino acids, which is quite different than free form arginine.

Second, meat tends to have plenty of carcingens in it which could induce colorectal tumorigenesis.

This research, once again, has very little relevance. This is just bad science.

I'm going to stop with these four because there is clearly a pattern developing here. Unless you can show the relevance of all this to healthy human subjects taking l-arginine, what you are doing here is hyping.

Yes, hyping. Hyping the possible negative effects of arginine supplementation. Posting a bunch of out-of-context quotes from non-relevant research doesn't do much for me.

You can't, for example, quote research that shows screwy NO regulation in people with auto-immune diseases, cancer, and whatnot, and extrapolate that to mean that arginine supplementation is a scam.

Now, let's take a look at some of the more relevant pieces of research-

1: J Physiol. 2007 Mar 8; [Epub ahead of print] Links
Inhibition of nitric oxide and prostaglandins, but not endothelial-derived hyperpolarizing factors, reduces blood flow and aerobic energy turnover in the exercising human leg.
· Mortensen SP,
· Gonzalez-Alonso J,
· Damsgaard R,
· Saltin B,
· Hellsten Y.
Copenhagen Muscle Research Centre.
Prostaglandins, nitric oxide (NO) and endothelial-derived hyperpolarizing factors (EDHFs) are substances that have been proposed to be involved in the regulation of skeletal muscle blood flow during physical activity. We measured hemodynamics, plasma ATP and VO2 at rest and during one-legged knee-extensor exercise (19+/-1 W) in 9 healthy subjects with and without intra-arterial infusion of indomethacin (INDO; 621+/-17 mg min(-1)), INDO + NG-monomethyl-L-arginine (L-NMMA; 12.4+/-0.3 mg min(-1))(Double) and INDO + L-NMMA + tetraethylammonium chloride (TEA; 12.4+/-0.3 mg min(-1))(Triple). Double and triple blockade lowered leg blood flow (LBF) at rest (P<0.05), while it remained unchanged with INDO. During exercise, LBF and vascular conductance were 2.54+/-0.10 l min(-1) and 25+/-1 mmHg, respectively, in control and they were lower with double (33+/-3 and 36+/-4%, respectively) and triple (26+/-4 and 28+/-3%, respectively) blockade (P<0.05), while there was no difference with INDO. The lower LBF and vascular conductance with double and triple blockade occurred in parallel with a lower O2 delivery, cardiac output, heart rate and plasma [norepinephrine] (P<0.05), while blood pressure remained unchanged and O2 extraction and femoral venous plasma [ATP] increased. Despite the increased O2 extraction, leg VO2 was 13 and 17% (triple and double, respectively) lower than control in parallel to a lower femoral venous temperature and lactate release (P<0.05). These results suggest that NO and prostaglandins play important roles in skeletal muscle blood flow regulation during moderate intensity exercise and that EDHFs do not compensate for the impaired formation of NO and prostaglandins. Moreover, inhibition of NO and prostaglandin formation is associated with a lower aerobic energy turnover and increased concentration of vasoactive ATP in plasma.

1: Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1407-11. Epub 2007 Jan 17. Links
Low-dose L-arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats.
· Ohta F,
· Takagi T,
· Sato H,
· Ignarro LJ.
Laboratory of Amino Acid Application, AminoScience Laboratories, Ajinomoto Co., Inc., 1-1 Suzuki-cho Kawasaki-ku, Kawasaki 210-8681, Japan. fumio_ohta@ajinomoto.com
The objective of this work was to evaluate the influence of exogenous L-arginine on the capillary blood flow of peripheral tissues of normotensive subjects. Rats were anesthetized with sodium pentobarbital, and the blood flow of femoral, dorsal, and ventral skin and gastrocnemius and soleus muscle was measured by laser Doppler flow and microsphere methods to compare the blood flow before and after the L-arginine infusion. L-arginine lowered the mean blood pressure in a dose-dependent manner, but a statistically significant reduction in mean blood pressure was detected only at a high dose of 500 mg/kg of body weight. The significant blood flow increment was detected after the L-arginine infusion at doses of 50 and 150 mg/kg without causing hypotension. Nicardipine, a calcium channel blocker, also increased the skin blood flow, but the blood flow increment and blood pressure fall were comparable. A significant increment in microperfusion was detected in gastrocnemius, soleus muscle, and ventral skin compared with control group by the microsphere method. No adverse effects were observed during L-arginine and microsphere infusion. The present work indicates that l-arginine infusion increases muscle capillary blood flow in rats that are not performing exercise. Supplementation with l-arginine might provide additional blood flow at rest and during exercise and result in the improvement of muscle performance and exercise capacity.
PMID: 17229841 [PubMed - indexed for MEDLINE]

1: J Appl Physiol. 2000 Apr;88(4):1192-8. Links
Nitric oxide synthase inhibition attenuates the skeletal muscle VEGF mRNA response to exercise.
· Gavin TP,
· Spector DA,
· Wagner H,
· Breen EC,
· Wagner PD.
Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623, USA. tgavin@ucsd.edu
Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta(1) (TGF-beta(1)) mRNA increase in rat skeletal muscle in response to a single acute exercise bout. Nitric oxide (NO) is released locally by muscle vascular endothelium and muscle fibers during exercise, contributes to the blood flow response to exercise, and regulates mitochondrial respiration. We hypothesized that a reduction in NO production, via NO synthase inhibition, would demonstrate a link between NO and the VEGF, bFGF, and TGF-beta(1) gene responses to exercise. To investigate this hypothesis, 9-wk-old female Wistar rats were divided into eight treatment groups (n = 6 each): 1) saline + rest, 2) saline + exercise, 3) 30 mg/kg N(omega)-nitro-L-arginine methyl ester (L-NAME, a known NOS inhibitor) + rest, 4) 30 mg/kg L-NAME + exercise, 5) 300 mg/kg L-NAME + rest, 6) 300 mg/kg L-NAME + exercise, 7) 300 mg/kg N(omega)-nitro-D-arginine methyl ester (D-NAME, inactive enantiomer of L-NAME) + rest, and 8) 300 mg/kg D-NAME + exercise. Exercise consisted of 1 h of running at 20 m/min on a 10 degrees incline. VEGF, TGF-beta(1), and bFGF mRNA from left gastrocnemius were analyzed by quantitative Northern blot. Submaximal exercise for 1 h increased VEGF mRNA 4.2-fold and TGF-beta(1) mRNA 1.5-fold in untreated rats but did not increase bFGF mRNA. The exercise-induced increase in VEGF mRNA was attenuated approximately 50% by 30 and 300 mg/kg L-NAME; the TGF-beta(1) mRNA increase was unaffected by 300 mg/kg L-NAME. In addition, 300 mg/kg D-NAME had no effect on the exercise-induced increase in VEGF mRNA. Administration of 300 mg/kg L-NAME had no effect on bFGF mRNA. These findings suggest that NO is important in the regulation of the VEGF gene response to exercise through increases in VEGF transcription or by increases in the VEGF mRNA half-life.
PMID: 10749807 [PubMed - indexed for MEDLINE

[Giantz11]

Well that should just about it do it.

Thank you and good night.

Good stuff Tony.

[MaDmaN]

Ok there you have the research, now lets see who felt that taking Arginine (AKG) 3,000mg's noticed any thing resembling the outrageous claims these companies made ?

I for one have not.

[poison]

That's the reply I was looking for. I tried to rep you, Tony.


Now, I'll say it again: IMO the arginine pump is purely cosmetic. I've never seen any lasting body composition changes from it, nor seen any effects whatsoever outside the pump.

I just don't believe it's gonna kill us.

[Sir Savage]

I do think some companies make some pretty outrageous claims about NO boosters, but I do think NO boosters offer some benefit, as well.

As some of y'all already mentioned, there's the cosmetic aspect of it. I for one think the cosmetic thing is pretty cool. I mean, let's face it- who doesn't want good pumps and hard wood, you feel me?

But I also think it goes beyond cosmetics, though. If you can increase blood flow, you can also increase nutrient flow. So if we boost NO via L-arginine, then we can get more glucose, creatine, and whatever else, to muscles.

I think few would argue that's not a good thing, right? Especially pre and post workout.

[T-Bone]

Originally Posted by Sir Savage

I do think some companies make some pretty outrageous claims about NO boosters, but I do think NO boosters offer some benefit, as well.

As some of y'all already mentioned, there's the cosmetic aspect of it. I for one think the cosmetic thing is pretty cool. I mean, let's face it- who doesn't want good pumps and hard wood, you feel me?

But I also think it goes beyond cosmetics, though. If you can increase blood flow, you can also increase nutrient flow. So if we boost NO via L-arginine, then we can get more glucose, creatine, and whatever else, to muscles.
I think few would argue that's not a good thing, right? Especially pre and post workout.

The bolded statement is the whole point of taking these types of products. At least for me it would be. Actually also the increased endurance is another reason.

[Mulletsoldier]

You must spread some Reputation around before giving it to Sir Savage again.

Couldn't have said it better myself. Literally.

[USPLabs]

Originally Posted by Sir Savage

I- who doesn't want good pumps and hard wood, you feel me?
.

Makes you feel that every workout is productive and it FEELS good to flex. I would take it just for that or what I call advanced placebo effect!

[poison]

I never got endurance from arginine. Citrulline is another story.

[john123131]

NO products are not for me personally, every product (no xplode, fasttwitch, horsepower, etc) leave my in the bathroom longer then in the gym!!...but........people love em, and some people swear by them. I get a much better pump from bcaa's and taurine pre/during then ive ever gotten from any no product. But to each there own, i know other products that work for me and not for others.
I dont think there dangerous, but there has been alot of controversy over them being a scam lately, i remember reading an article on t-mag a while ago about it too, but i base all of my supps off of personal trial rather then claims and review articles anyway

[Cosmo Kramer]

Originally Posted by Sir Savage

But I also think it goes beyond cosmetics, though. If you can increase blood flow, you can also increase nutrient flow. So if we boost NO via L-arginine, then we can get more glucose, creatine, and whatever else, to muscles.

I agree but most of the aspects of recovery are rate limited.

To put it simply, if you stick all the materials to build a house in front of a construction company at once, they are still limited to how fast they can build it.

The more I look at it, as long as adequate amounts are present, the difference between a moderate amount to a large amount is almost nil.


But it can't hurt and sure does look good

[Sir Savage]

Originally Posted by Bobo

I agree but most of the aspects of recovery are rate limited.

To put it simply, if you stick all the materials to build a house in front of a construction company at once, they are still limited to how fast they can build it.

The more I look at it, as long as adequate amounts are present, the difference between a moderate amount to a large amount is almost nil.

Yeah.

But I look at it like this- using the house analogy, you have to have all the necessary materials present to build a strong, solid house.

Similarly, you need to have all the materials present to build a strong, solid body- AAKG for NO, creatine, taurine, etc. Make sure all the bases are covered, IMO, to get that extra benefit.

[poopypants]

wow great thread! thanks for reading it for me!!! i was bout to say never would i think that pumpin my muscles full a blood and getting raging wood was a bad thing..... reps to you savage... NO hype ..... get a job lol j/p

[NO HYPE]

Supplemental arginine's role as the one and only NO substrate, is not in question here.... it's the hype that accompanies the claims of the NO products.

Originally Posted by NO HYPE

The entire premise behind NO products, is NO up-regulation.... IF the NO products even aquired the ability to up-regulate endogenous NO production (wich they don't)....

It would be detrimental to our health!

Does everyone understand that in healthy adults, any significant up-regulation of endogenous NO concentrations.... results in the augmentation of physiological homeostasis, and initiates many adverse, cytotoxic reactions?

The NO products are backed by outrageous claims, when in fact they are nothing more than vasodilators.... but one of the claims is, sustained up-regulation of NO (and all of the benefits that accompany it's up-regulation).

The adverse effects of increased NO concentrations are definitely not discussed by the companies making the NO products (yet their claim of NO up-regulation is always accompanied by beneficial babble).... hence the reason why I posted excerpts indicating just a portion of the adverse effects caused by NO up-regulation.

Supplemental arginine is a great addition for maintaining it's endogenous role as a NO substrate however, these NO products (as much as the hype indicates otherwise), do not even aquire the ability to significantly up-regulate NO.

Originally Posted by NO HYPE

In healthy adults (provided there is no shortage of the NO substrate), there is no need for NO up-regulation, and if there were a need.... it would not be possible to significantly up-regulate via the oral arginine-based "NO products", due to the p53-mediated, regulatory negative feedback loop.

[NO HYPE]

Here's something you won't find in NO advertisements....

The primary trigger for iNOS is inflammatory response.... which is excactly what eccentric exercise induces. (Entrez PubMed)

iNOS is induced by inflammatory cytokines in skeletal muscle.

[NO HYPE]

Originally Posted by Giantz11

Well that should just about it do it.

Thank you and good night.

No, I don't think so.... sweet dreams.:

[NO HYPE]

Originally Posted by poison

That's the reply I was looking for. I tried to rep you, Tony.

.... figures.

[NO HYPE]

Originally Posted by poison

I just don't believe it's gonna kill us.

Kill us?

Who mentioned anything about NO killing us?

[NO HYPE]

Originally Posted by Sir Savage

I do think some companies make some pretty outrageous claims about NO boosters, but I do think NO boosters offer some benefit, as well.

As some of y'all already mentioned, there's the cosmetic aspect of it. I for one think the cosmetic thing is pretty cool. I mean, let's face it- who doesn't want good pumps and hard wood, you feel me?

But I also think it goes beyond cosmetics, though. If you can increase blood flow, you can also increase nutrient flow. So if we boost NO via L-arginine, then we can get more glucose, creatine, and whatever else, to muscles.

I think few would argue that's not a good thing, right? Especially pre and post workout.

It's kind of funny how after all the marketing hype.... that the majority of people realize that the "NO" products are simply "cosmetic" vasodilators.

[NO HYPE]

Originally Posted by Sir Savage

I do think some companies make some pretty outrageous claims about NO boosters,. but I do think NO boosters offer some benefit, as well.

.... BINGO.

[Cosmo Kramer]

Originally Posted by Sir Savage

Yeah.

But I look at it like this- using the house analogy, you have to have all the necessary materials present to build a strong, solid house.

Similarly, you need to have all the materials present to build a strong, solid body- AAKG for NO, creatine, taurine, etc. Make sure all the bases are covered, IMO, to get that extra benefit.

The necessary materials are pretty straight forward.

[NO HYPE]

Originally Posted by Sir Savage

I do think some companies make some pretty outrageous claims about NO boosters, but I do think NO boosters offer some benefit, as well.

Like what.... great pumps and attenuated GH levels in response to exercise?

Oral arginine attenuates the growth hormone response to resistance exercise -- Collier et al. 101 (3): 848 -- Journal of Applied Physiology

[Cosmo Kramer]

Can you please chill on the colored and bolded fonts?